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The platelets begin to clump together, become spiked and sticky, and bind to the exposed collagen and endothelial lining.

This process is assisted by a glycoprotein in the blood plasma called von Willebrand factor, which helps stabilize the growing platelet plug. As platelets collect, they simultaneously release chemicals from their granules into the plasma that further contribute to hemostasis.

The process is sometimes characterized as a cascade, because one event prompts the next as in a multi-level waterfall.

The result is the production of a gelatinous but robust clot made up of a mesh of Fibrin—an insoluble filamentous protein derived from fibrinogen, the plasma protein introduced earlier—in which platelets and blood cells

In large, randomized controlled trials, significantly reduced perioperative blood loss compared with placebo in a variety of surgical procedures, including cardiac surgery with or without cardiopulmonary bypass, total hip and knee replacement and prostatectomy, gynecological procedures.

The plasma protein binding of tranexamic acid is about 3% at therapeutic plasma levels and seems to be fully accounted for by its binding to plasminogen (does not bind serum albumin).

Pass the Blood Brain Barrier

In patients with hereditary angioedema, inhibition of the formation and activity of plasmin by tranexamic acid may prevent attacks of angioedema by decreasing plasmin-induced activation of the first complement protein (C1).

To determine if pre-hospital administration of TXA in trauma patients with signs of hemorrhagic shock provides for a statistically significant decrease in mortality, total blood product usage and total estimated blood loss, without a significant increase in thromboembolic complications